Oncogene activation of HIV-LTR-driven expression via the NF-kappa B binding sites.

Abstract:

:The Raf-1 proto-oncogene product is a highly regulated serine/threonine kinase that functions in signal transduction downstream from growth factor receptors and upstream from nuclear proto-oncogene products. Using a transient cotransfection assay we have found that activated Raf-1 activates expression from the HIV-LTR. Analysis of a series of 5' deletion and point mutations revealed the NF-kappa B motifs as the Raf-responsive element in the HIV-LTR. Moreover, Raf-BXB activated expression from heterologous promoters driven by the HIV NF-kappa B binding sites. In addition to Raf, we show that v-Src, v-H-Ras and v-Mos activate HIV-LTR expression through the NF-kappa B binding sites and v-H-Ras-induced HIV-LTR expression is mediated by Raf-1. These findings may have implications for the involvement of the cellular homologues of these oncogenes in the switch from latent to productive infection by HIV in response to T-cell activation.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Bruder JT,Heidecker G,Tan TH,Weske JC,Derse D,Rapp UR

doi

10.1093/nar/21.22.5229

subject

Has Abstract

pub_date

1993-11-11 00:00:00

pages

5229-34

issue

22

eissn

0305-1048

issn

1362-4962

journal_volume

21

pub_type

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